Temporal-parietal-occipital epilepsy in GEFS+ associated with SCN1A mutation.
GEFS+
SCN1A
epilepsy
neural networks
post-ictal migraine
temporal-parietal-occipital
Journal
Epileptic disorders : international epilepsy journal with videotape
ISSN: 1950-6945
Titre abrégé: Epileptic Disord
Pays: United States
ID NLM: 100891853
Informations de publication
Date de publication:
01 Apr 2021
01 Apr 2021
Historique:
pubmed:
15
4
2021
medline:
15
12
2021
entrez:
14
4
2021
Statut:
ppublish
Résumé
Most families with genetic epilepsy with febrile seizures plus show a mutation in the sodium channel alpha 1 subunit gene, however, but there is much phenotypic heterogeneity and focal epilepsy remains relatively rare. Here, we report a family with electroclinical features indicative of temporal-parietal-occipital carrefour epilepsy with common occurrence of post-ictal migraine. We studied a four-generation family including nine affected subjects by means of EEG and MRI. Genetic testing was performed by targeted re-sequencing (gene panel). In most patients, seizure semiology included cognitive, autonomic, and emotional symptoms, eventually evolving towards sensory visual phenomena. Focal sensory vestibular seizures and changes in body perception were also reported in some cases. Post-ictal migraine was common, occurring in five out of the six (83%) epilepsy patients. A missense mutation (c.1130 G>A; p.R377Q) affecting the S5-S6 segment (pore region) of the sodium channel alpha 1 subunit was identified in all affected and four unaffected subjects. Temporal-parietal-occipital carrefour epilepsy is part of the genetic epilepsy with febrile seizures plus spectrum. The electroclinical features in this family support the involvement of a genetically impaired neural network. High prevalence of post-ictal migraine suggests the role of posterior brain areas in the clinical expression of this gene defect.
Identifiants
pubmed: 33851920
pii: epd.2021.1266
doi: 10.1684/epd.2021.1266
doi:
Substances chimiques
NAV1.1 Voltage-Gated Sodium Channel
0
SCN1A protein, human
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM